Sex is a costly habit. Current evolutionary thought holds that sex is ubiquitous among successful species and conserved for its evolutionary benefits: When the environment grows harsh, a sexually reproducing species can trade its genes around, trying for a better hand of cards. But—here’s the rub—sex also produces fewer offspring over the long term than clonal reproduction. A sexually reproducing female has only half the fitness of an asexual female, a phenomenon biologist John Maynard Smith described as the two-fold cost of sex. It’s no wonder the question of how useful and widespread sex really is—the question of why it has been maintained—has troubled everyone from Richard Dawkins (“The evolution of sex…that problem of problems”) to Graham Bell (“Sex is the queen of problems in evolutionary biology.”). Now scientists studying yeast, a group that includes some of the most scrutinized sexual cycles in biology, are finding that the hardest thing may be just telling whether sex is even happening.

Biologists collaborating with the Broad Institute’s Fungal Genome Initiative were hoping to see genes for sexual cell division, called meiosis, in eight newly sequenced genomes. Though yeast sex is difficult to watch live—one recent project had to simulate all the conditions of human skin to get the fungi to “get it on”—observing the distribution of alleles in a population and seeing whether spores, usually a product of meiosis, are formed, can suggest whether sexual recombination is at work. On the basis of spore formation, Joseph Heitman and Jennifer Reedy of Duke University considered two of the species, Candida lusitaniae and C. guilliermondii, candidates for sexual cell division. The researchers were poised to see whether the genomes agreed. What they found was remarkable: Although all population-level signs pointed to sexual recombination, those two species of yeast each lacked dozens of genes previously considered crucial for meiosis.

Heitman and Reedy’s research suggests we know less about the genetic underpinnings of yeast sex than we thought we did. Our present knowledge rests on the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, the major model organisms in the study of eukaryote genetics. They have clear meiotic cycles. In these and almost all other yeast, a gene called the mating-type locus determines whether a cell is one of two mating types. When two cells of different mating types come in close vicinity, the cells grow extensions called shmoos that fuse to form a cell with a double dose of DNA. This “double” form is stable until environmental stresses trigger meiosis, causing the sexual cycle to repeat.

Comparisons of the genomes of those yeast with the genome of C. albicans, the most common pathogenic yeast, yielded what geneticists had considered the “meiotic toolbox,” the genes necessary for yeast sex. C. albicans has a parasexual cycle, which involves two cells fusing to produce the “double” form and then a gradual loss of chromosomes until the normal number is restored. That parasexual cycle, geneticists thought, was due to the absence of some genes necessary for meiosis.

Unfortunately for proponents of the toolbox argument, C. lusitaniae and C. guilliermondii have even fewer of the genes putatively necessary for meiosis than C. albicans does. Nevertheless, C. lusitaniae and C. guilliermondii do seem to be having meiotic sex. The one gene all three share is for an enzyme called SPO11, which seems to cause meiotic recombination in all studied organisms. It’s possible, says Heitman, that in C.albicans SPO11 has been reconfigured to cause recombination without meiosis. If so, the presence of SPO11 may indicate that C. albicans has developed a way to reap the benefits of recombination without having a meiotic sexual cycle.

But if some yeast have developed an alternative pathway to meiotic recombination, using any standard meiotic genes as a sex diagnostic may no longer make sense. Genes used for one purpose in one species may have evolved into a different use in another, notes John Logsdon of University of Iowa, who studies the evolution of meiosis. Meiotic genes in one species may be playing different roles in another.

To unravel why sex exists, we must first identify the species where it does happen. If those genes cannot be depended on, a new diagnostic may be in order—we might even go back to the basics. “[Though] sex is often the escape pathway, and most species have sex when things are bad, it’s traditional to catch them in the act,” says Logsdon. “I keep telling my colleagues, ‘You just need to catch them doing it.’”